The proposed research is designed to examine the significance of identifiable biochemical aberrations to abnormal polymorphonuclear leukocyte function in patients with major thermal trauma. To document the relationship of leukocyte dysfunction to sepsis in these patients and to establish the role of such PMN dysfunction in non-burn trauma. The contribution of both oxidative and non-oxidative mechanisms to this important host defense system will be examined. Serial measurements of NBT reduction, O2 consumption, NAD (P) H oxidase activity, O2., superoxide dismutase, H2O2 and myeloperoxidase activity will be performed in thermal injury and non-burn trauma patients as well as in normal controls. In addition, the roles of glutathione, glutathione peroxidase, catalase, and glucose-6-phosphate dehydrogenase will be examined. It is hoped through identification of these abnormalities and isolation of responsible agents, that better preventive and/or corrective treatment regimens can be devised for these patients.